Previous work demonstrated a threshold for paraplegia in dogs subjected to chronic cervical cord compression. Animals with systemic arterial perfusion pressure above threshold were protected from graded compression, while those with subthreshold perfusion pressure were not. Further, compression of the spinal cord at two or more levels, as in human cervical spondylosis, reduced the critical perfusion threshold below that for a single level. We believe, therefore, that cervical spondylosis may produce myelopathy by compression first, and by rendering it more susceptible to ischemia second. We propose to establish chronic vascular insufficiency of the cervical spinal cord in the dog to test the relative importance of compression and ischemia. The experimental model will include 1) multiple paraspinal arterial occlusion effecting cord ischemia, 2) maximal tolerable cord compression anteriorly at C4 and C5, and 3) a combination of ischemia and cord compression. Spinal cord blood flow will be measured by Xenon133 washout and by colloidal carbon black in order to establish the role of ischemia in chronic spondylotic myelopathy. Both the distribution of blood to and the autoregulatory function of the compressed cord will be assessed. Abnormal flow patterns and loss of autoregulation will verify the role of regional ischemia in cervical spondylotic myelopathy.